PMID- 15339774 OWN - NLM STAT- MEDLINE DCOM- 20041202 LR - 20091026 IS - 0029-7844 (Print) IS - 0029-7844 (Linking) VI - 104 IP - 3 DP - 2004 Sep TI - Transmission of parentally shared human leukocyte antigen alleles and the risk of preterm delivery. PG - 594-600 AB - OBJECTIVE: Our objective was to examine our hypothesis that the transmission of parentally shared human leukocyte antigen (HLA) alleles to offspring increases the risk of preterm delivery. METHODS: A population-based family study with participating children and their parents was conducted in Kaiser Permanente Medical Care Program, an integrated healthcare delivery system, in the Northern California Region. A total of 234 participants from 78 families with early preterm deliveries (35 weeks of gestation or greater) and 60 participants from 20 families with full-term births were included in the study. Buccal cells were collected from the first-born preterm cases and their parents to determine HLA-B (class I) and DRB1 (class II) types and the transmission of parental alleles to the offspring. The buccal samples were also collected from full-term deliveries to rule out possible segregation distortion at the studied HLA loci. RESULTS: Compared with the expected transmission probability based on Mendel's laws (25%), transmission of parentally shared HLA-B or DRB1 alleles from both heterozygous parents to offspring (48% of 23 heterozygous parents) was associated with a more than 5-fold increased risk of preterm delivery (odds ratio 5.5; 95% confidence interval 1.2-51). Transmission of parentally shared HLA alleles from heterozygous mothers (83%) appears to be more important in the etiology of preterm delivery than transmission from fathers (57%). The transmission pattern of parentally shared HLA alleles in our full-term controls was almost identical to the expected pattern based on Mendel's laws and demonstrated no segregation distortion at those HLA loci. CONCLUSION: Our findings provide evidence that the transmission of parentally shared HLA alleles may be an underlying mechanism for preterm delivery. FAU - Li, De-Kun AU - Li DK AD - Division of Research, Kaiser Permanente, Oakland, California 94612, USA. dkl@dor.kaiser.org FAU - Odouli, Roxana AU - Odouli R FAU - Liu, Liyan AU - Liu L FAU - Vinson, Margaret AU - Vinson M FAU - Trachtenberg, Elizabeth AU - Trachtenberg E LA - eng GR - 2 M01 RR01271-21/RR/NCRR NIH HHS/United States PT - Journal Article PT - Research Support, Non-U.S. Gov't PT - Research Support, U.S. Gov't, P.H.S. PL - United States TA - Obstet Gynecol JT - Obstetrics and gynecology JID - 0401101 RN - 0 (HLA Antigens) SB - IM MH - Alleles MH - Female MH - HLA Antigens/*immunology MH - Humans MH - *Maternal-Fetal Exchange MH - Obstetric Labor, Premature/*immunology MH - Pregnancy MH - Risk Factors EDAT- 2004/09/02 05:00 MHDA- 2004/12/16 09:00 CRDT- 2004/09/02 05:00 PHST- 2004/09/02 05:00 [pubmed] PHST- 2004/12/16 09:00 [medline] PHST- 2004/09/02 05:00 [entrez] AID - 104/3/594 [pii] AID - 10.1097/01.AOG.0000130067.27022.1d [doi] PST - ppublish SO - Obstet Gynecol. 2004 Sep;104(3):594-600. doi: 10.1097/01.AOG.0000130067.27022.1d.